Lanlan Yu

Alcohol consumption increases the risk of gastritis and gastric ulcer. Nutritional alternatives are considered for relieving the progression of gastric mucosal lesions instead of conventional drugs that produce side effects. This study was designed to evaluate the gastroprotective effects and investigate the defensive mechanisms of wheat peptides against ethanol-induced acute gastric mucosal injury in rats. Sixty male Sprague-Dawley rats were divided into six groups and orally treated with wheat peptides (0.1, 0.2, 0.4 g/kgbw) and omeprazole (20 mg/kgbw) for 4 weeks, following absolute ethanol administration for 1 h. Pretreatment with wheat peptides obviously enhanced the vasodilation of gastric mucosal blood vessels via improving the gastric mucosal blood flow and elevating the defensive factors nitric oxide (NO) and prostaglandin E2 (PGE2), and lowering the level of vasoconstrictor factor endothelin (ET)-1. Wheat peptides exhibited anti-inflammatory reaction through decreasing inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and increasing trefoil factor 1 (TFF1) levels. Moreover, wheat peptides significantly down-regulated the expression of phosphorylated nuclear factor kappa-B (p-NF-κB) p65 proteins in the NF-κB signaling pathway. Altogether, wheat peptides protect gastric mucosa from ethanol-induced lesions in rats via improving the gastric microcirculation and inhibiting inflammation mediated by the NF-κB signaling transduction pathway.

The influences of maternal fine particulate matter (PM2.5) exposure on intestinal oxidative stress, inflammation, tight junctions, and gut microbiota of offspring are not well understood. Moreover, research on the dietary intervention method has not been well studied. In our study, dams received PM2.5 and quercetin intervention during gestation and lactation, and then inflammation biomarkers, oxidative stress indicators, tight junction proteins, and gut microbiota in the colon of offspring were analyzed. Compared with the control group, lower catalase (CAT) and superoxide dismutase (SOD) activities, higher interleukin-17A (IL-17A) and interleukin-22 (IL-22), decreased ZO-1 and occludin expressions, and higher Bacteroides abundance were observed in the offspring mice of the PM2.5 group. However, higher CAT and SOD activities, lower IL-17A and IL-22 levels, increased ZO-1 and occludin expressions, and lower Bacteroides abundance were found in the quercetin groups. In addition, there was a negative correlation between Bacteroides abundance and CAT concentration. Additionally, Bacteroides abundance was positively related to IL-17A and IL-22 levels. These findings suggest that maternal PM2.5 exposure may have some certain effects on intestinal oxidative stress, inflammation, and tight junctions. Quercetin administration may protect the offspring against these adverse effects. Changes of Bacteroides abundance play an important role in the process.